Asset Details
Do you wish to reserve the book?
Ferulic acid inhibits nitric oxide-induced apoptosis by enhancing GABA81 receptor expression in transient focal cerebral ischemia in rats
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Ferulic acid inhibits nitric oxide-induced apoptosis by enhancing GABA81 receptor expression in transient focal cerebral ischemia in rats
Do you wish to request the book?
Ferulic acid inhibits nitric oxide-induced apoptosis by enhancing GABA81 receptor expression in transient focal cerebral ischemia in rats
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Ferulic acid inhibits nitric oxide-induced apoptosis by enhancing GABA81 receptor expression in transient focal cerebral ischemia in rats
2010
Overview
Aim： Ferulic acid （4-hydroxy-3-methoxycinnamic acid, FA） provides neuroprotection against apoptosis in a transient middle cerebral artery occlusion （MCAo） model. This study was to further investigate the anti-apoptotic effect of FA during reperfusion after cerebral ischemia. Methods： Rats were subjected to 90 min of cerebral ischemia followed by 3 or 24 h of reperfusion after which they were sacrificed. Results： Intravenous FA （100 mg/kg） administered immediately after middle cerebral artery occlusion （MCAo） or 2 h after reperfusion effectively abrogated the elevation of postsynaptic density-95 （PSD-95）, neuronal nitric oxide synthase （nNOS）, inducible nitric oxide synthase （iNOS）, nitrotyrosine, and cleaved caspase-3 levels as well as apoptosis in the ischemic cortex at 24 h of reperfusion. FA fur- ther inhibited Bax translocation, cytochrome c release, and p38 mitogen-activated protein （MAP） kinase phosphorylation. Moreover, FA enhanced the expression of gamma-aminobutyric acid type B receptor subunit 1 （GABAB1） in the ischemic cortex at 3 and 24 h of reperfusion. In addition, nitrotyrosine-positive cells colocalized with cleaved caspase-3-positive cells, and phospho-p38 MAP kinase- positive cells cotocalized with nitrotyrosine- and Bax-positive cells, indicating a positive relationship among the expression of nitroty- rosine, phospho-p38 MAP kinase, Bax, and cleaved caspase-3. The mutually exclusive expression of GABA81and nitrotyrosine revealed that there is a negative correlation between GABAB1 and nitrotyrosine expression profiles. Additionally, pretreatment with saclofen, a GABAe receptor antagonist, abolished the neuroprotection of FA against nitric oxide （NO）-induced apoptosis. Conclusion： FA significantly enhances GABAB1 receptor expression at early reperfusion and thereby provides neuroprotection against p38 MAP kinase-mediated NO-induced apoptosis at 24 h of reperfusion.
We currently cannot retrieve any items related to this title. Kindly check back at a later time.